Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation Research
Search: search_blue_button Advanced Search
Circulation Research. 2000;87:179-183

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Irani, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Irani, K.
Related Collections
Right arrow Apoptosis
Right arrow Cell signalling/signal transduction
Right arrow Growth factors/cytokines
Right arrow Smooth muscle proliferation and differentiation
Right arrow Endothelium/vascular type/nitric oxide
(Circulation Research. 2000;87:179.)
© 2000 American Heart Association, Inc.


MiniReview

Oxidant Signaling in Vascular Cell Growth, Death, and Survival

A Review of the Roles of Reactive Oxygen Species in Smooth Muscle and Endothelial Cell Mitogenic and Apoptotic Signaling

Kaikobad Irani

From The Johns Hopkins University School of Medicine, Baltimore, Md.

Correspondence to Kaikobad Irani, MD, The Johns Hopkins University School of Medicine, Ross 1023, 720 Rutland Ave, Baltimore, MD 21205. E-mail kirani{at}mail.jhmi.edu


*    Abstract
up arrowTop
*Abstract
down arrowIntroduction
down arrowSmooth Muscle Cells
down arrowEndothelial Cells
down arrowSources of ROS in...
down arrowPotential Targets of ROS...
down arrowThe Answer to the...
down arrowSummary
down arrowReferences
 
Abstract—Reactive oxygen species (ROS) have been traditionally regarded as toxic byproducts of aerobic metabolism. However, ROS can also act as intracellular signaling molecules in vascular cells. ROS can mediate phenotypes in vascular endothelial and smooth muscle cells that may be considered both physiological and pathophysiological. Among these are growth, apoptosis, and survival. The specific response elicited by reactive oxygen intermediaries is determined by their specific intracellular target(s). This, in turn, is dependent on the species of oxidant(s) produced, the source and therefore subcellular localization of the oxidant(s), the kinetics of production, and the quantities produced. A fuller understanding of how ROS regulate mitogenesis and apoptosis in vascular smooth muscle and endothelial cells will permit the development of novel strategies to modify or prevent vascular diseases in which these phenotypes predominate.


Key Words: reactive oxygen species • intracellular signaling


*    Introduction
up arrowTop
up arrowAbstract
*Introduction
down arrowSmooth Muscle Cells
down arrowEndothelial Cells
down arrowSources of ROS in...
down arrowPotential Targets of ROS...
down arrowThe Answer to the...
down arrowSummary
down arrowReferences
 
This MiniReview is part of a thematic series on Oxidant Signaling in Cardiovascular Cells, which includes the following articles: NAD(P)H Oxidase: Role in Cardiovascular Biology and Disease

Oxidant Signaling in Vascular Cell Growth, Death, and Survival

Antiatherogenic Mechanisms of Antioxidants Crosstalk Between Nitric Oxide and Lipid Oxidation Systems: Implications for Vascular Disease Oxygen Radicals and Endothelial Dysfunction Vascular Oxygen Species Generation

David G. Harrison, Guest Editor

Many cells that comprise the vasculature generate reactive oxygen species (ROS). Conventional thought has generally regarded these elementary molecules as harmful to the vasculature, leading to such pathological processes as hypertension, restenosis, and atherosclerosis. However, controlled clinical trials have failed to show a consistent benefit of antioxidants on atherosclerotic disease and its sequelae.1 2 3 Although a number of factors may contribute to this lack of efficacy, one intriguing possibility is that ROS through their many effects on vascular cells play both a physiological and pathophysiological role in vascular homeostasis. The purpose of this review is to summarize the varied effects that ROS have on vascular smooth muscle and endothelial cell growth, death, and survival. The pertinent redox-sensitive targets of ROS in these cells that mediate these effects will be discussed. Finally, a hypothesis for the mechanism(s) by which ROS result in diverse phenotypes in endothelial and smooth muscle cells will be presented.


*    Smooth Muscle Cells
up arrowTop
up arrowAbstract
up arrowIntroduction
*Smooth Muscle Cells
down arrowEndothelial Cells
down arrowSources of ROS in...
down arrowPotential Targets of ROS...
down arrowThe Answer to the...
down arrowSummary
down arrowReferences
 
Vascular smooth muscle cell (SMC) accumulation and hypertrophy are characteristic of atherosclerotic, restenotic, and hypertensive vascular diseases (reviewed in Reference 4 ). The net balance between proliferation and apoptosis determines the extent of SMC growth.

Proliferation
SMCs respond to growth factor stimulation with intracellular production of ROS. Such ligands include those acting via tyrosine kinase receptors such as platelet-derived growth factor (PDGF)5 and G protein–coupled receptors such as phenylephrine6 and thrombin.7 For instance, PDGF, a mitogen implicated in atherogenesis, stimulates the production of H2O2 in vascular SMCs and leads to SMC growth. Suppression of the PDGF-stimulated rise in H2O2 blunts this proliferative response. Similarly, thrombin stimulates H2O2 and superoxide production in SMCs.7 Suppression of these ROS by treatment with catalase or superoxide dismutase inhibits thrombin-induced mitogenesis. Finally, stimulation of SMCs with phenylephrine leads to induction of H2O2, suppression of which inhibits phenylephrine-induced proliferation.6

A role for ROS, especially H2O2, in SMC growth is further supported by the finding that exogenous H2O2 or chemical agents that generate ROS induce tyrosine phosphorylation of mitogen-activated protein kinases, and cell growth.5 8 9 10 Taken together, these studies strongly suggest that ROS, and H2O2 in particular, mediate the proliferative phenotype in vascular SMCs.

Survival
In parallel to their important role in SMC proliferation, ROS have also been shown to be necessary for SMC survival. Suppression of endogenous intracellular H2O2, through overexpression of catalase or treatment with membrane-permeable antioxidants, not only inhibits proliferation but also promotes apoptosis in SMCs.11 12 Thus, ROS, and H2O2 in particular, act as signaling intermediaries in antiapoptotic pathways in vascular SMCs.

Hypertrophy
Angiotensin II (Ang II), a proinflammatory mediator implicated in atherosclerosis, restenosis, and hypertension,13 leads to the hypertrophic response in SMCs via the production of both superoxide and H2O2 and activation of p38 MAPK.14 15 Suppression of ROS inhibits Ang II–induced hypertrophy. Thus, ROS have also been linked with Ang II–induced pathological SMC hypertrophy.

Apoptosis and Growth Arrest
ROS, in addition to acting as growth-promoting signaling molecules, can also suppress growth and/or lead to programmed cell death in SMCs. Overexpression of the tumor suppressor gene p53 leads to an increase in ROS in SMCs, growth inhibition, and/or apoptosis.16 Furthermore, suppression of p53-induced ROS abrogates p53-induced apoptosis. Thus, in the context of p53-regulated cell-cycle progression, ROS are negative regulators of vascular SMC growth and survival. The physiological significance of these findings is supported by studies showing that p53 is an important endogenous regulator of SMC growth, and that inactivation of p53 is strongly associated with pathological SMC proliferation in human restenotic lesions.17

Other studies using exogenously generated oxidants have similarly reported that ROS lead to cell death of SMCs.18 19 Interestingly, some of these studies have shown that exposure of SMCs to relatively low levels of oxidant stress for short periods promotes growth, whereas prolonged exposure to higher concentrations leads to cell death. Moreover, the species of oxidant added was important in determining the fate of the cell: superoxide resulted in cell growth whereas H2O2 led to cell death.


*    Endothelial Cells
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowSmooth Muscle Cells
*Endothelial Cells
down arrowSources of ROS in...
down arrowPotential Targets of ROS...
down arrowThe Answer to the...
down arrowSummary
down arrowReferences
 
Endothelial cell (EC) growth, death, and function are important determinants of vascular homeostasis.

Apoptosis
Although a causative role for EC apoptosis in the pathogenesis of vascular diseases has not been proven, mounting evidence shows that EC loss is a prominent feature of human atherosclerosis.20 Apoptotic ECs become procoagulant.21 In addition, the importance of EC apoptosis in atherogenesis and the role of ROS in this process are supported by studies showing that many risk factors for vascular disease promote apoptotic death of ECs through redox-dependent signaling. These include oxidized LDL and lipoprotein(a),22 23 24 high glucose and insulin,25 26 and Ang II.27 28 Moreover, ROS have been implicated in EC anoikis.29 Thus, ROS may play an important role in mediating apoptotic death in ECs that lose their interaction with the subendothelial matrix as seen at sites of atherosclerosis and those exposed to proatherogenic factors.

Survival
Although the role of ROS in promoting endothelial dysfunction and death has been well studied, the role of endogenously generated ROS in EC survival is relatively unknown. In nonvascular cells, superoxide production regulated by the small GTPase Rac1 protects against apoptosis.30 Similarly, recent evidence from our laboratory also points toward a crucial role for ROS generated by a Rac1-regulated oxidase in suppressing EC death via activation of nuclear factor-{kappa}B, whereas ROS produced independent of Rac1 promote EC apoptosis.31 Thus, by most accounts, endothelial production of ROS leads to cell death or promotes dysfunction. On the other hand, ROS specifically produced by a Rac1-regulated oxidase appear to prevent apoptosis of ECs.

The TableDown summarizes the role of ROS in SMC and EC growth, apoptosis, and survival.


View this table:
[in this window]
[in a new window]
 
Table 1. Summary of References in This Review Supporting Different Roles of ROS in SMC and EC Growth, Apoptosis, and Survival


*    Sources of ROS in SMCs and ECs: The Importance of an NAD(P)H Oxidase
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowSmooth Muscle Cells
up arrowEndothelial Cells
*Sources of ROS in...
down arrowPotential Targets of ROS...
down arrowThe Answer to the...
down arrowSummary
down arrowReferences
 
The observation that SMCs and ECs are capable of producing ROS has spurred a great deal of interest in identifying the enzymatic source(s) of these oxidants. A variety of cellular enzymes are potential candidates, including those involved in arachidonic acid metabolism, microsomal cytochrome P-450, xanthine oxidase, and mitochondrial electron transport. Arguably the most exciting recent discovery in this area is that ECs and SMCs possess an NAD(P)H oxidase activity analogous to the multicomponent phagocyte NADPH oxidase. The functional characteristics of this oxidase and its importance in cardiovascular biology and disease are covered in much greater detail in another review in this thematic series.32 Suffice it to say that many, although not all, components of this oxidase have been identified at the RNA or protein levels in SMCs and ECs.7 33 34 35 36 37 In addition, Rac1, a small GTPase that is an essential regulatory component of the phagocyte oxidase,38 is ubiquitously expressed.


*    Potential Targets of ROS in ECs and SMCs
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowSmooth Muscle Cells
up arrowEndothelial Cells
up arrowSources of ROS in...
*Potential Targets of ROS...
down arrowThe Answer to the...
down arrowSummary
down arrowReferences
 
The list of intracellular targets of ROS is growing rapidly. A detailed review of this list is beyond the scope of this article. However, within the context of vascular cell growth and apoptosis, certain names merit particular attention (FigureDown).



View larger version (20K):
[in this window]
[in a new window]
 
Figure 1. Schematic illustrating the potential sources and molecular targets of ROS in the context of SMC and EC growth, apoptosis, and survival. Interdependence and interactions between different ROS sources and signaling proteins are not shown.

Extracellular Signal–Regulated Kinases
The mitogen-activated protein kinase (MAPK) family, also known as extracellular signal–regulated kinases (ERKs), is activated by exogenous H2O2 and by endogenously generated ROS in SMCs stimulated with growth factors.5 ERKs are important mediators of proliferation. Activation of ERKs has also been implicated in vascular endothelial growth factor (VEGF)–induced EC survival.39

Stress-Activated Protein Kinases
Kinases belonging to the stress-activated protein kinase (SAPK) family, which include c-Jun N-terminal kinases (JNKs) and p38 MAPK, are also sensitive to redox modulation (reviewed in Reference 40 ). Members of the Rho family of small GTPases including Rac1 regulate these kinases.40 In contrast to ERKs, JNKs and their downstream target c-Jun, have been implicated in H2O2 and other stress-induced apoptosis of ECs.41 42 Moreover, p38 MAPK has been implicated in EC upregulation of intercellular adhesion molecule-1 and, therefore, endothelial dysfunction.43 In SMCs, redox-sensitive activation of p38 MAPK mediates Ang II–induced hypertrophy14 and has also been implicated in SMC migration.44

Nuclear Factor-{kappa}B (NF-{kappa}B)
Activation of the transcription factor NF-{kappa}B has been associated with EC dysfunction and vascular inflammation.45 NF-{kappa}B–mediated transcription is also important in cell survival (reviewed in Reference 46 ). The activation of NF-{kappa}B by ROS, specifically ROS generated by a Rac1-regulated NAD(P)H oxidase, has been shown in HeLa cells.47 In SMCs, constitutive activation of NF-{kappa}B has been reported to be essential for proliferation.48 In addition, Ang II–induced effects on SMCs may also be mediated via NF-{kappa}B.49 In ECs, NF-{kappa}B is a prime target for ROS, and its activation has been linked to EC dysfunction (reviewed in Reference 45 ) and survival.31 50 51 52 53

Akt Kinase
Akt is a kinase, which lies downstream of phosphoinositide 3-kinase (PI 3-kinase), and is involved in antiapoptotic signaling (reviewed in Reference 54 ). It is regulated by ROS in Ang II–stimulated SMCs.55 In ECs, activation of Akt has been linked to the protective effects of shear stress56 and VEGF-induced growth and survival.57 58 59 Rac1 is a target for the products of PI 3-kinase,60 implicating a Rac1-regulated, NAD(P)H-dependent oxidase in the signaling pathways involving Akt in ECs and SMCs.

Caspases
Caspases are cysteine proteases that execute the apoptotic message. Caspases are sensitive to redox changes in the cell (reviewed in Reference 61 ). Specifically, in ECs, processing and activity of the downstream caspase-3 in response to cell detachment29 or tumor necrosis factor (TNF) stimulation31 are regulated by ROS.

It is worth emphasizing that many of the signaling proteins mentioned above that are sensitive to the redox state of the cell may not be direct targets of ROS. In fact, it is very likely that one or more intermediary proteins are involved. Tyrosine phosphatases are prime candidates for such intermediaries. Such phosphatases all have redox-sensitive cysteine residues in their active sites,62 which are essential for their biological activity.63 The generally accepted paradigm is that an increase in intracellular ROS by inhibiting tyrosine phosphatase activity transiently tips the balance toward tyrosine kinases that then leads to phosphorylation of their cellular targets, such as ERKs and SAPKs.


*    The Answer to the Paradox: What, Where, How, and How Much?
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowSmooth Muscle Cells
up arrowEndothelial Cells
up arrowSources of ROS in...
up arrowPotential Targets of ROS...
*The Answer to the...
down arrowSummary
down arrowReferences
 
The studies reviewed above show that ROS generated within vascular SMCs and ECs can either induce cell growth or arrest or promote survival or death, thereby leading to vascular dysfunction or acting as mediators of physiological vascular function. Although recently appreciated in vascular biology, such apparently paradoxical roles of ROS have been recognized in other fields of biology. The explanation to this paradox has been hinted at in the studies reviewed above and is probably a combination of the following factors:

  1. What: The Species of Oxidant(s) Produced and the Proportion of Different Oxidant Species. Certain highly reactive oxidant species such as ·OH and peroxynitrite are more cytotoxic than others (reviewed in Reference 64 ). Moreover, ROS have differential effects on cellular targets such as ERKs10 and on cell growth.18 Thus, the redox milieu of the cell including its iron content and expression of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, and catalase, which play an important part in determining the species and amounts of ROS, is probably a key factor in determining the response of a cell to ROS production.
  2. Where: The Subcellular Localization of the ROS. Similar to nitric oxide synthases, oxidoreductases are spatially distributed in a selective fashion,65 effectively controlling access of targets for ROS produced from different intracellular sources.
  3. How: The Kinetics of ROS Production. The kinetics of oxidant production could differentially activate and/or inhibit targets such as transcription factors, resulting in a host of cellular responses. Such differential activation of transcription factors allows the cell to use the same second messenger to elicit varied responses and is known to exist for other well-known second messengers systems such as Ca2+.66
  4. How Much: The Amplitude of ROS Production. The quantities of ROS produced probably have a profound effect in determining the fate of the cell. This is supported by observations that activation of specific redox-sensitive kinases such as ERKs and p38 MAPK in SMCs is very dependent on the concentration of ROS.5 14


*    Summary
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowSmooth Muscle Cells
up arrowEndothelial Cells
up arrowSources of ROS in...
up arrowPotential Targets of ROS...
up arrowThe Answer to the...
*Summary
down arrowReferences
 
The experimental data to date suggest potential conflicting roles of oxidants in the genesis of vascular disorders. This presents a challenge to scientists and clinicians alike. It is imperative that future efforts be directed toward better defining and characterizing the signaling pathways regulated by ROS in vascular cells. Such efforts will likely yield new molecular targets and ultimately more effective therapies for preventing or ameliorating vascular diseases such as atherosclerosis, restenosis, and hypertension, through fine modulation of ROS-regulated signaling.


*    Acknowledgments
 
This review was supported by The Johns Hopkins University Clinician Scientist Award, The W.W. Smith Charitable Trust, the Mid-Atlantic American Heart Association, the Bernard Foundation, and the Abraham and Virginia Weiss Endowment. I thank C.J. Lowenstein for constructive criticism of this manuscript. I also thank my collaborators P.J. Goldschmidt-Clermont and T. Finkel and all the members of my laboratory for helpful comments and discussions.


*    Footnotes
 
This manuscript was sent to Donald D. Heistad, Consulting Editor, for review by expert referees, editorial decision, and final disposition.

Received March 10, 2000; accepted June 19, 2000.


*    References
up arrowTop
up arrowAbstract
up arrowIntroduction
up arrowSmooth Muscle Cells
up arrowEndothelial Cells
up arrowSources of ROS in...
up arrowPotential Targets of ROS...
up arrowThe Answer to the...
up arrowSummary
*References
 
1. Rapola JM, Virtamo J, Ripatti S, Huttunen JK, Albanes D, Taylor PR, Heinonen OP. Randomised trial of alpha-tocopherol and beta-carotene supplements on incidence of major coronary events in men with previous myocardial infraction. Lancet. 1997;349:1715–1720.[Medline] [Order article via Infotrieve]

2. Stephens NG, Parsons A, Schofield PM, Kelly F, Cheeseman K, Mitchinson MJ. Randomised controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study (CHAOS). Lancet. 1996;347:781–786.[Medline] [Order article via Infotrieve]

3. Yusuf S, Dagenais G, Pogue J, Bosch J, Sleight P. Vitamin E supplementation and cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med. 2000;342:154–160.[Abstract/Free Full Text]

4. Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature. 1993;362:801–809.[Medline] [Order article via Infotrieve]

5. Sundaresan M, Yu ZX, Ferrans VJ, Irani K, Finkel T. Requirement for generation of H2O2 for platelet-derived growth factor signal transduction. Science. 1995;270:296–299.[Abstract/Free Full Text]

6. Nishio E, Watanabe Y. The involvement of reactive oxygen species and arachidonic acid in {alpha}1-adrenoceptor-induced smooth muscle cell proliferation and migration. Br J Pharmacol. 1997;121:665–670.[Medline] [Order article via Infotrieve]

7. Patterson C, Ruef J, Madamanchi NR, Barry-Lane P, Hu Z, Horaist C, Ballinger CA, Brasier AR, Bode C, Runge MS. Stimulation of a vascular smooth muscle cell NAD(P)H oxidase by thrombin. Evidence that p47(phox) may participate in forming this oxidase in vitro and in vivo. J Biol Chem. 1999;274:19814–19822.[Abstract/Free Full Text]

8. Rao GN, Lassegue B, Griendling KK, Alexander RW. Hydrogen peroxide stimulates transcription of c-Jun in vascular smooth muscle cells: role of arachidonic acid. Oncogene. 1993;8:2759–2764.[Medline] [Order article via Infotrieve]

9. Rao GN, Berk BC. Active oxygen species stimulate vascular smooth muscle cell growth and proto-oncogene expression. Circ Res. 1992;70:593–599.[Abstract/Free Full Text]

10. Baas AS, Berk BC. Differential activation of mitogen-activated protein kinases by H2O2 and O2- in vascular smooth muscle cells. Circ Res. 1995;77:29–36.[Abstract/Free Full Text]

11. Tsai JC, Jain M, Hsieh CM, Lee WS, Yoshizumi M, Patterson C, Perrella MA, Cooke C, Wang H, Haber E, Schlegel R, Lee ME. Induction of apoptosis by pyrrolidine dithiocarbamate and N-acetylcysteine in vascular smooth muscle cells. J Biol Chem. 1996;271:3667–3670.[Abstract/Free Full Text]

12. Brown MR, Miller FJ Jr, Li WG, Ellingson AN, Mozena JD, Chatterjee P, Engelhardt JF, Zwacka RM, Oberley LW, Fang X, Spector AA, Weintraub NL. Overexpression of human catalase inhibits proliferation and promotes apoptosis in vascular smooth muscle cells. Circ Res. 1999;85:524–533.[Abstract/Free Full Text]

13. Alexander RW. Theodore Cooper Memorial Lecture. Hypertension and the pathogenesis of atherosclerosis. Oxidative stress and the mediation of arterial inflammatory response: a new perspective. Hypertension. 1995;25:155–161.[Abstract/Free Full Text]

14. Ushio-Fukai M, Alexander RW, Akers M, Griendling KK. p38 Mitogen-activated protein kinase is a critical component of the redox-sensitive signaling pathways activated by angiotensin II. Role in vascular smooth muscle cell hypertrophy. J Biol Chem. 1998;273:15022–15029.[Abstract/Free Full Text]

15. Zafari AM, Ushio-Fukai M, Akers M, Yin Q, Shah A, Harrison DG, Taylor WR, Griendling KK. Role of NADH/NADPH oxidase-derived H2O2 in angiotensin II–induced vascular hypertrophy. Hypertension. 1998;32:488–495.[Abstract/Free Full Text]

16. Johnson TM, Yu ZX, Ferrans VJ, Lowenstein RA, Finkel T. Reactive oxygen species are downstream mediators of p53-dependent apoptosis. Proc Natl Acad Sci U S A. 1996;93:11848–11852.[Abstract/Free Full Text]

17. Speir E, Modali R, Huang ES, Leon MB, Shawl F, Finkel T, Epstein SE. Potential role of human cytomegalovirus and p53 interaction in coronary restenosis. Science. 1994;265:391–394.[Abstract/Free Full Text]

18. Li PF, Dietz R, von Harsdorf R. Differential effect of hydrogen peroxide and superoxide anion on apoptosis and proliferation of vascular smooth muscle cells. Circulation. 1997;96:3602–3609.[Abstract/Free Full Text]

19. Li PF, Dietz R, von Harsdorf R. Reactive oxygen species induce apoptosis of vascular smooth muscle cell. FEBS Lett. 1997;404:249–252.[Medline] [Order article via Infotrieve]

20. Davies MJ, Woolf N, Rowles PM, Pepper J. Morphology of the endothelium over atherosclerotic plaques in human coronary arteries. Br Heart J. 1988;60:459–464.[Abstract/Free Full Text]

21. Bombeli T, Karsan A, Tait JF, Harlan JM. Apoptotic vascular endothelial cells become procoagulant. Blood. 1997;89:2429–2442.[Abstract/Free Full Text]

22. Li D, Yang B, Mehta JL. Ox-LDL induces apoptosis in human coronary artery endothelial cells: role of PKC, PTK, bcl-2, and Fas. Am J Physiol. 1998;275:H568–H576.[Abstract/Free Full Text]

23. Galle J, Heermeier K, Wanner C. Atherogenic lipoproteins, oxidative stress, and cell death. Kidney Int Suppl. 1999;71:S62–S65.[Medline] [Order article via Infotrieve]

24. Dimmeler S, Haendeler J, Galle J, Zeiher AM. Oxidized low-density lipoprotein induces apoptosis of human endothelial cells by activation of CPP32-like proteases. A mechanistic clue to the "response to injury" hypothesis. Circulation. 1997;95:1760–1763.[Abstract/Free Full Text]

25. Du XL, Sui GZ, Stockklauser-Färber K, Weiss J, Zink S, Schwippert B, Wu QX, Tschöpe D, Rösen P. Introduction of apoptosis by high proinsulin and glucose in cultured human umbilical vein endothelial cells is mediated by reactive oxygen species. Diabetologia. 1998;41:249–256.[Medline] [Order article via Infotrieve]

26. Du X, Stocklauser-Färber K, Rösen P. Generation of reactive oxygen intermediates, activation of NF-{kappa}B, and induction of apoptosis in human endothelial cells by glucose: role of nitric oxide synthase? Free Radic Biol Med. 1999;27:752–763.[Medline] [Order article via Infotrieve]

27. Dimmeler S, Rippmann V, Weiland U, Haendeler J, Zeiher AM. Angiotensin II induces apoptosis of human endothelial cells: protective effect of nitric oxide. Circ Res. 1997;81:970–976.[Abstract/Free Full Text]

28. Li D, Yang B, Philips MI, Mehta JL. Proapoptotic effects of ANG II in human coronary artery endothelial cells: role of AT1 receptor and PKC activation. Am J Physiol. 1999;276:H786–H792.[Abstract/Free Full Text]

29. Li AE, Ito H, Rovira, II, Kim KS, Takeda K, Yu ZY, Ferrans VJ, Finkel T. A role for reactive oxygen species in endothelial cell anoikis. Circ Res. 1999;85:304–310.[Abstract/Free Full Text]

30. Joneson T, Bar-Sagi D. Suppression of ras-induced apoptosis by the rac GTPase. Mol Cell Biol. 1999;19:5892–5901.[Abstract/Free Full Text]

31. Deshpande SS, Angkeow P, Huang J, Ozaki M, Irani K. Rac1 inhibits TNF-{alpha}-induced endothelial cell apoptosis: dual regulation by reactive oxygen species. FASEB J. In press.

32. Griendling KK, Sorescu D, Ushio-Fukai M. NAD(P)H oxidase: role in cardiovascular biology and disease. Circ Res. 2000;86:494–501.[Abstract/Free Full Text]

33. Fukui T, Lassegue B, Kai H, Alexander RW, Griendling KK. Cytochrome b-558 {alpha}-subunit cloning and expression in rat aortic smooth muscle cells. Biochim Biophys Acta. 1995;1231:215–219.[Medline] [Order article via Infotrieve]

34. Bayraktutan U, Draper N, Lang D, Shah AM. Expression of functional neutrophil-type NADPH oxidase in cultured rat coronary microvascular endothelial cells. Cardiovasc Res. 1998;38:256–262.[Abstract/Free Full Text]

35. Jones SA, O’Donnell VB, Wood JD, Broughton JP, Hughes EJ, Jones OT. Expression of phagocyte NADPH oxidase components in human endothelial cells. Am J Physiol. 1996;271:H1626–H1634.[Abstract/Free Full Text]

36. Archer SL, Reeve HL, Michelakis E, Puttagunta L, Waite R, Nelson DP, Dinauer MC, Weir EK. O2 sensing is preserved in mice lacking the gp91 phox subunit of NADPH oxidase. Proc Natl Acad Sci U S A. 1999;96:7944–7949.[Abstract/Free Full Text]

37. Suh YA, Arnold RS, Lassegue B, Shi J, Xu X, Sorescu D, Chung AB, Griendling KK, Lambeth JD. Cell transformation by the superoxide-generating oxidase Mox1. Nature. 1999;401:79–82.[Medline] [Order article via Infotrieve]

38. Abo A, Pick E, Hall A, Totty N, Teahan CG, Segal AW. Activation of the NADPH oxidase involves the small GTP-binding protein p21rac1. Nature. 1991;353:668–670.[Medline] [Order article via Infotrieve]

39. Gupta K, Kshirsagar S, Li W, Gui L, Ramakrishnan S, Gupta P, Law PY, Hebbel RP. VEGF prevents apoptosis of human microvascular endothelial cells via opposing effects on MAPK/ERK and SAPK/JNK signaling. Exp Cell Res. 1999;247:495–504.[Medline] [Order article via Infotrieve]

40. Kyriakis JM, Avruch J. Sounding the alarm: protein kinase cascades activated by stress and inflammation. J Biol Chem. 1996;271:24313–24316.[Free Full Text]

41. Wang N, Verna L, Hardy S, Zhu Y, Ma KS, Birrer MJ, Stemerman MB. c-Jun triggers apoptosis in human vascular endothelial cells. Circ Res. 1999;85:387–393.[Abstract/Free Full Text]

42. Verheij M, Bose R, Lin XH, Yao B, Jarvis WD, Grant S, Birrer MJ, Szabo E, Zon LI, Kyriakis JM, Haimovitz-Friedman A, Fuks Z, Kolesnick RN. Requirement for ceramide-initiated SAPK/JNK signaling in stress-induced apoptosis. Nature. 1996;380:75–79.[Medline] [Order article via Infotrieve]

43. Tamura DY, Moore EE, Johnson JL, Zallen G, Aiboshi J, Silliman CC. p38 Mitogen-activated protein kinase inhibition attenuates intercellular adhesion molecule-1 up-regulation on human pulmonary microvascular endothelial cells. Surgery. 1998;124:403–407.[Medline] [Order article via Infotrieve]

44. Hedges JC, Dechert MA, Yamboliev IA, Martin JL, Hickey E, Weber LA, Gerthoffer WT. A role for p38(MAPK)/HSP27 pathway in smooth muscle cell migration. J Biol Chem. 1999;274:24211–24219.[Abstract/Free Full Text]

45. Collins T. Endothelial nuclear factor-{kappa}B and the initiation of the atherosclerotic lesion. Lab Invest. 1993;68:499–508.[Medline] [Order article via Infotrieve]

46. Baichwal VR, Baeuerle PA. Activate NF-{kappa}B or die? Curr Biol. 1997;7:R94–R96.[Medline] [Order article via Infotrieve]

47. Sulciner DJ, Irani K, Yu ZX, Ferrans VJ, Goldschmidt-Clermont P, Finkel T. rac1 Regulates a cytokine-stimulated, redox-dependent pathway necessary for NF-{kappa}B activation. Mol Cell Biol. 1996;16:7115–7121.[Abstract]

48. Bellas RE, Lee JS, Sonenshein GE. Expression of a constitutive NF-{kappa}B-like activity is essential for proliferation of cultured bovine vascular smooth muscle cells. J Clin Invest. 1995;96:2521–2527.

49. Kranzhöfer R, Schmidt J, Pfeiffer CA, Hagl S, Libby P, Kübler W. Angiotensin induces inflammatory activation of human vascular smooth muscle cells. Arterioscler Thromb Vasc Biol. 1999;19:1623–1629.[Abstract/Free Full Text]

50. Cooper JT, Stroka DM, Brostjan C, Palmetshofer A, Bach FH, Ferran C. A20 blocks endothelial cell activation through a NF-{kappa}B-dependent mechanism. J Biol Chem. 1996;271:18068–18073.[Abstract/Free Full Text]

51. Scatena M, Almeida M, Chaisson ML, Fausto N, Nicosia RF, Giachelli CM. NF-{kappa}B mediates {alpha}vß3 integrin-induced endothelial cell survival. J Cell Biol. 1998;141:1083–1093.[Abstract/Free Full Text]

52. Stehlik C, de Martin R, Kumabashiri I, Schmid JA, Binder BR, Lipp J. Nuclear factor (NF)-{kappa}B-regulated X-chromosome-linked iap gene expression protects endothelial cells from tumor necrosis factor {alpha}-induced apoptosis. J Exp Med. 1998;188:211–216.[Abstract/Free Full Text]

53. Zen K, Karsan A, Stempien-Otero A, Yee E, Tupper J, Li X, Eunson T, Kay MA, Wilson CB, Winn RK, Harlan JM. NF-{kappa}B activation is required for human endothelial survival during exposure to tumor necrosis factor-{alpha} but not to interleukin-1ß or lipopolysaccharide. J Biol Chem. 1999;274:28808–28815.[Abstract/Free Full Text]

54. Downward J. Mechanisms and consequences of activation of protein kinase B/Akt. Curr Opin Cell Biol. 1998;10:262–267.[Medline] [Order article via Infotrieve]

55. Ushio-Fukai M, Alexander RW, Akers M, Yin Q, Fujio Y, Walsh K, Griendling KK. Reactive oxygen species mediate the activation of Akt/protein kinase B by angiotensin II in vascular smooth muscle cells. J Biol Chem. 1999;274:22699–22704.[Abstract/Free Full Text]

56. Dimmeler S, Assmus B, Hermann C, Haendeler J, Zeiher AM. Fluid shear stress stimulates phosphorylation of Akt in human endothelial cells: involvement in suppression of apoptosis. Circ Res. 1998;83:334–341.[Abstract/Free Full Text]

57. Fujio Y, Walsh K. Akt mediates cytoprotection of endothelial cells by vascular endothelial growth factor in an anchorage-dependent manner. J Biol Chem. 1999;274:16349–16354.[Abstract/Free Full Text]

58. Gerber HP, McMurtrey A, Kowalski J, Yan M, Keyt BA, Dixit V, Ferrara N. Vascular endothelial growth factor regulates endothelial cell survival through the phosphatidylinositol 3'-kinase/Akt signal transduction pathway. Requirement for Flk-1/KDR activation. J Biol Chem. 1998;273:30336–30343.[Abstract/Free Full Text]

59. Wu LW, Mayo LD, Dunbar JD, Kessler KM, Baerwald MR, Jaffe EA, Wang D, Warren RS, Donner DB. Utilization of distinct signaling pathways by receptors for vascular endothelial cell growth factor and other mitogens in the induction of endothelial cell proliferation. J Biol Chem. 2000;275:5096–5103.[Abstract/Free Full Text]

60. Han J, Luby-Phelps K, Das B, Shu X, Xia Y, Mosteller RD, Krishna UM, Falck JR, White MA, Broek D. Role of substrates and products of PI 3-kinase in regulating activation of Rac-related guanosine triphosphatases by Vav. Science. 1998;279:558–560.[Abstract/Free Full Text]

61. Hampton MB, Fadeel B, Orrenius S. Redox regulation of the caspases during apoptosis. Ann N Y Acad Sci. 1998;854:328–335.[Medline] [Order article via Infotrieve]

62. Fischer EH, Charbonneau H, Tonks NK. Protein tyrosine phosphatases: a diverse family of intracellular and transmembrane enzymes. Science. 1991;253:401–406.[Abstract/Free Full Text]

63. Hecht D, Zick Y. Selective inhibition of protein tyrosine phosphatase activities by H2O2 and vanadate in vitro. Biochem Biophys Res Commun. 1992;188:773–779.[Medline] [Order article via Infotrieve]

64. Naqui A, Chance B, Cadenas E. Reactive oxygen intermediates in biochemistry. Annu Rev Biochem. 1986;55:137–166.[Medline] [Order article via Infotrieve]

65. Cross AR, Jones OT. Enzymic mechanisms of superoxide production. Biochim Biophys Acta. 1991;1057:281–298.[Medline] [Order article via Infotrieve]

66. Dolmetsch RE, Lewis RS, Goodnow CC, Healy JI. Differential activation of transcription factors induced by Ca2+ response amplitude and duration [published correction appears in Nature. 1997;388:308]. Nature. 1997;386:855–858.




This article has been cited by other articles:


Home page
HypertensionHome page
H. Li, W. Han, V. A. M. Villar, L. B. Keever, Q. Lu, U. Hopfer, M. T. Quinn, R. A. Felder, P. A. Jose, and P. Yu
D1-Like Receptors Regulate NADPH Oxidase Activity and Subunit Expression in Lipid Raft Microdomains of Renal Proximal Tubule Cells
Hypertension, June 1, 2009; 53(6): 1054 - 1061.
[Abstract] [Full Text] [PDF]


Home page
Arterioscler. Thromb. Vasc. Bio.Home page
M. Y. Lee, A. S. Martin, P. K. Mehta, A. E. Dikalova, A. M. Garrido, S. R. Datla, E. Lyons, K.-H. Krause, B. Banfi, J. D. Lambeth, et al.
Mechanisms of Vascular Smooth Muscle NADPH Oxidase 1 (Nox1) Contribution to Injury-Induced Neointimal Formation
Arterioscler Thromb Vasc Biol, April 1, 2009; 29(4): 480 - 487.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
Y. Lin, X. Liu, Y. Cheng, J. Yang, Y. Huo, and C. Zhang
Involvement of MicroRNAs in Hydrogen Peroxide-mediated Gene Regulation and Cellular Injury Response in Vascular Smooth Muscle Cells
J. Biol. Chem., March 20, 2009; 284(12): 7903 - 7913.
[Abstract] [Full Text] [PDF]


Home page
PhysiologyHome page
S. Hou, S. H. Heinemann, and T. Hoshi
Modulation of BKCa Channel Gating by Endogenous Signaling Molecules
Physiology, February 1, 2009; 24(1): 26 - 35.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
J. Li, X.-L. Niu, and N. R. Madamanchi
Leukocyte Antigen-related Protein Tyrosine Phosphatase Negatively Regulates Hydrogen Peroxide-induced Vascular Smooth Muscle Cell Apoptosis
J. Biol. Chem., December 5, 2008; 283(49): 34260 - 34272.
[Abstract] [Full Text] [PDF]


Home page
Circ. Res.Home page
J. Kisucka, A. K. Chauhan, I. S. Patten, A. Yesilaltay, C. Neumann, R. A. Van Etten, M. Krieger, and D. D. Wagner
Peroxiredoxin1 Prevents Excessive Endothelial Activation and Early Atherosclerosis
Circ. Res., September 12, 2008; 103(6): 598 - 605.
[Abstract] [Full Text] [PDF]


Home page
Am J Trop Med HygHome page
S. Rajendiran, H. S. Lakshamanappa, B. Zachariah, and S. Nambiar
Desialylation of Plasma Proteins in Severe Dengue Infection: Possible Role of Oxidative Stress
Am J Trop Med Hyg, September 1, 2008; 79(3): 372 - 377.
[Abstract] [Full Text] [PDF]


Home page
FASEB J.Home page
S. Yuan, Y. Fu, X. Wang, H. Shi, Y. Huang, X. Song, L. Li, N. Song, and Y. Luo
Voltage-dependent anion channel 1 is involved in endostatin-induced endothelial cell apoptosis
FASEB J, August 1, 2008; 22(8): 2809 - 2820.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Cell Physiol.Home page
L. Ai, M. Rouhanizadeh, J. C. Wu, W. Takabe, H. Yu, M. Alavi, R. Li, Y. Chu, J. Miller, D. D. Heistad, et al.
Shear stress influences spatial variations in vascular Mn-SOD expression: implication for LDL nitration
Am J Physiol Cell Physiol, June 1, 2008; 294(6): C1576 - C1585.
[Abstract] [Full Text] [PDF]


Home page
IOVSHome page
Y. Saito, A. Uppal, G. Byfield, S. Budd, and M. E. Hartnett
Activated NAD(P)H Oxidase from Supplemental Oxygen Induces Neovascularization Independent of VEGF in Retinopathy of Prematurity Model
Invest. Ophthalmol. Vis. Sci., April 1, 2008; 49(4): 1591 - 1598.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
W. Han, H. Li, V. A. M. Villar, A. M. Pascua, M. I. Dajani, X. Wang, A. Natarajan, M. T. Quinn, R. A. Felder, P. A. Jose, et al.
Lipid Rafts Keep NADPH Oxidase in the Inactive State in Human Renal Proximal Tubule Cells
Hypertension, February 1, 2008; 51(2): 481 - 487.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Renal Physiol.Home page
G. Ding, A. Zhang, S. Huang, X. Pan, G. Zhen, R. Chen, and T. Yang
ANG II induces c-Jun NH2-terminal kinase activation and proliferation of human mesangial cells via redox-sensitive transactivation of the EGFR
Am J Physiol Renal Physiol, December 1, 2007; 293(6): F1889 - F1897.
[Abstract] [Full Text] [PDF]


Home page
J. Physiol.Home page
P. Newsholme, E. P. Haber, S. M. Hirabara, E. L. O. Rebelato, J. Procopio, D. Morgan, H. C. Oliveira-Emilio, A. R. Carpinelli, and R. Curi
Diabetes associated cell stress and dysfunction: role of mitochondrial and non-mitochondrial ROS production and activity
J. Physiol., August 15, 2007; 583(1): 9 - 24.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
J. Ryu, C. W. Lee, J.-A. Shin, C.-S. Park, J. J. Kim, S.-J. Park, and K. H. Han
Fc{gamma}RIIa mediates C-reactive protein-induced inflammatory responses of human vascular smooth muscle cells by activating NADPH oxidase 4
Cardiovasc Res, August 1, 2007; 75(3): 555 - 565.
[Abstract] [Full Text] [PDF]


Home page
J. Exp. Biol.Home page
C. Gaitanaki, T. Kalpachidou, I.-K. S. Aggeli, P. Papazafiri, and I. Beis
CoCl2 induces protective events via the p38-MAPK signalling pathway and ANP in the perfused amphibian heart
J. Exp. Biol., July 1, 2007; 210(13): 2267 - 2277.
[Abstract] [Full Text] [PDF]


Home page
J. Appl. Physiol.Home page
P. H. McNulty, B. J. Robertson, M. A. Tulli, J. Hess, L. A. Harach, S. Scott, and L. I. Sinoway
Effect of hyperoxia and vitamin C on coronary blood flow in patients with ischemic heart disease
J Appl Physiol, May 1, 2007; 102(5): 2040 - 2045.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
S. Horke, I. Witte, P. Wilgenbus, M. Kruger, D. Strand, and U. Forstermann
Paraoxonase-2 Reduces Oxidative Stress in Vascular Cells and Decreases Endoplasmic Reticulum Stress-Induced Caspase Activation
Circulation, April 17, 2007; 115(15): 2055 - 2064.
[Abstract] [Full Text] [PDF]


Home page
Arterioscler. Thromb. Vasc. Bio.Home page
S. Bonello, C. Zahringer, R. S. BelAiba, T. Djordjevic, J. Hess, C. Michiels, T. Kietzmann, and A. Gorlach
Reactive Oxygen Species Activate the HIF-1{alpha} Promoter Via a Functional NF{kappa}B Site
Arterioscler Thromb Vasc Biol, April 1, 2007; 27(4): 755 - 761.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
A. Alcaraz, D. Iyu, N. M. Atucha, J. Garcia-Estan, and M. C. Ortiz
Vitamin E supplementation reverses renal altered vascular reactivity in chronic bile duct-ligated rats
Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2007; 292(4): R1486 - R1493.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
G. Cambonie, B. Comte, C. Yzydorczyk, T. Ntimbane, N. Germain, N. L. O. Le, P. Pladys, C. Gauthier, I. Lahaie, D. Abran, et al.
Antenatal antioxidant prevents adult hypertension, vascular dysfunction, and microvascular rarefaction associated with in utero exposure to a low-protein diet
Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2007; 292(3): R1236 - R1245.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
E. Anselm, M. Chataigneau, M. Ndiaye, T. Chataigneau, and V. B. Schini-Kerth
Grape juice causes endothelium-dependent relaxation via a redox-sensitive Src- and Akt-dependent activation of eNOS
Cardiovasc Res, January 15, 2007; 73(2): 404 - 413.
[Abstract] [Full Text] [PDF]


Home page
Physiol. Rev.Home page
K. Bedard and K.-H. Krause
The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology
Physiol Rev, January 1, 2007; 87(1): 245 - 313.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Cell Mol. Bio.Home page
Y. Wang, M. M. Zeigler, G. K. Lam, M. G. Hunter, T. D. Eubank, V. V. Khramtsov, S. Tridandapani, C. K. Sen, and C. B. Marsh
The Role of the NADPH Oxidase Complex, p38 MAPK, and Akt in Regulating Human Monocyte/Macrophage Survival
Am. J. Respir. Cell Mol. Biol., January 1, 2007; 36(1): 68 - 77.
[Abstract] [Full Text] [PDF]


Home page
Eur. J. Cardiothorac. Surg.Home page
E. Gurbanov and X. Shiliang
The key role of apoptosis in the pathogenesis and treatment of pulmonary hypertension.
Eur. J. Cardiothorac. Surg., September 1, 2006; 30(3): 499 - 507.
[Abstract] [Full Text] [PDF]


Home page
Arterioscler. Thromb. Vasc. Bio.Home page
K. R. Brunt, K. K. Fenrich, G. Kiani, M. Yat Tse, S. C. Pang, C. A. Ward, and L. G. Melo
Protection of Human Vascular Smooth Muscle Cells From H2O2-Induced Apoptosis Through Functional Codependence Between HO-1 and AKT
Arterioscler Thromb Vasc Biol, September 1, 2006; 26(9): 2027 - 2034.
[Abstract] [Full Text] [PDF]


Home page
HeartHome page
R Waksman, I M Leitch, J Roessler, H Yazdi, R Seabron, F Tio, R W Scott, R I Grove, S Rychnovsky, B Robinson, et al.
Intracoronary photodynamic therapy reduces neointimal growth without suppressing re-endothelialisation in a porcine model
Heart, August 1, 2006; 92(8): 1138 - 1144.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
L. Moldovan, K. Mythreye, P. J. Goldschmidt-Clermont, and L. L. Satterwhite
Reactive oxygen species in vascular endothelial cell motility. Roles of NAD(P)H oxidase and Rac1
Cardiovasc Res, July 15, 2006; 71(2): 236 - 246.
[Abstract] [Full Text] [PDF]


Home page
J BiochemHome page
O. Zschenker, T. Illies, and D. Ameis
Overexpression of lysosomal Acid lipase and other proteins in atherosclerosis.
J. Biochem., July 1, 2006; 140(1): 23 - 38.
[Abstract] [Full Text] [PDF]


Home page
J. Leukoc. Biol.Home page
A. Vega, P. Chacon, G. Alba, R. El Bekay, J. Monteseirin, J. Martin-Nieto, and F. Sobrino
Modulation of IgE-dependent COX-2 gene expression by reactive oxygen species in human neutrophils
J. Leukoc. Biol., July 1, 2006; 80(1): 152 - 163.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Renal Physiol.Home page
L. Xia, H. Wang, H. J. Goldberg, S. Munk, I. G. Fantus, and C. I. Whiteside
Mesangial cell NADPH oxidase upregulation in high glucose is protein kinase C dependent and required for collagen IV expression
Am J Physiol Renal Physiol, February 1, 2006; 290(2): F345 - F356.
[Abstract] [Full Text] [PDF]


Home page
JCBHome page
K. Matsushita, C. N. Morrell, R. J.A. Mason, M. Yamakuchi, F. A. Khanday, K. Irani, and C. J. Lowenstein
Hydrogen peroxide regulation of endothelial exocytosis by inhibition of N-ethylmaleimide sensitive factor
J. Cell Biol., July 4, 2005; 170(1): 73 - 79.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
W. Zhang, S. Zheng, P. Storz, and W. Min
Protein Kinase D Specifically Mediates Apoptosis Signal-regulating Kinase 1-JNK Signaling Induced by H2O2 but Not Tumor Necrosis Factor
J. Biol. Chem., May 13, 2005; 280(19): 19036 - 19044.
[Abstract] [Full Text] [PDF]


Home page
Toxicol SciHome page
P.-C. Lee, I-C. Ho, and T.-C. Lee
Oxidative Stress Mediates Sodium Arsenite-Induced Expression of Heme Oxygenase-1, Monocyte Chemoattractant Protein-1, and Interleukin-6 in Vascular Smooth Muscle Cells
Toxicol. Sci., May 1, 2005; 85(1): 541 - 550.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
P. K. Aley, K. E. Porter, J. P. Boyle, P. J. Kemp, and C. Peers
Hypoxic Modulation of Ca2+ Signaling in Human Venous Endothelial Cells: MULTIPLE ROLES FOR REACTIVE OXYGEN SPECIES
J. Biol. Chem., April 8, 2005; 280(14): 13349 - 13354.
[Abstract] [Full Text] [PDF]


Home page
Mol. Cell. Biol.Home page
J.-M. Li, L. M. Fan, M. R. Christie, and A. M. Shah
Acute Tumor Necrosis Factor Alpha Signaling via NADPH Oxidase in Microvascular Endothelial Cells: Role of p47phox Phosphorylation and Binding to TRAF4
Mol. Cell. Biol., March 15, 2005; 25(6): 2320 - 2330.
[Abstract] [Full Text] [PDF]


Home page
Arterioscler. Thromb. Vasc. Bio.Home page
S.-J. Lin, S.-K. Shyue, Y.-Y. Hung, Y.-H. Chen, H.-H. Ku, J.-W. Chen, K.-B. Tam, and Y.-L. Chen
Superoxide Dismutase Inhibits the Expression of Vascular Cell Adhesion Molecule-1 and Intracellular Cell Adhesion Molecule-1 Induced by Tumor Necrosis Factor-{alpha} in Human Endothelial Cells Through the JNK/p38 Pathways
Arterioscler Thromb Vasc Biol, February 1, 2005; 25(2): 334 - 340.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Endocrinol. Metab.Home page
B. D. Fink, K. J. Reszka, J. A. Herlein, M. M. Mathahs, and W. I. Sivitz
Respiratory uncoupling by UCP1 and UCP2 and superoxide generation in endothelial cell mitochondria
Am J Physiol Endocrinol Metab, January 1, 2005; 288(1): E71 - E79.
[Abstract] [Full Text] [PDF]


Home page
Am J Trop Med HygHome page
L. GIL, G. MARTINEZ, R. TAPANES, O. CASTRO, D. GONZALEZ, L. BERNARDO, S. VAZQUEZ, G. KOURI, and M. G. GUZMAN
OXIDATIVE STRESS IN ADULT DENGUE PATIENTS
Am J Trop Med Hyg, November 1, 2004; 71(5): 652 - 657.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
J.-M. Li and A. M Shah
Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology
Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2004; 287(5): R1014 - R1030.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
C. Zhang, J. Yang, and L. K. Jennings
Attenuation of neointima formation through the inhibition of DNA repair enzyme PARP-1 in balloon-injured rat carotid artery
Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H659 - H666.
[Abstract] [Full Text] [PDF]


Home page
J. Am. Soc. Nephrol.Home page
L. Zeng, H. Xu, T.-L. Chew, R. Chisholm, M. M. Sadeghi, Y. S. Kanwar, and F. R. Danesh
Simvastatin Modulates Angiotensin II Signaling Pathway by Preventing Rac1-Mediated Upregulation of p27
J. Am. Soc. Nephrol., July 1, 2004; 15(7): 1711 - 1720.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
J. F. Wang, X. Zhang, and J. E. Groopman
Activation of Vascular Endothelial Growth Factor Receptor-3 and Its Downstream Signaling Promote Cell Survival under Oxidative Stress
J. Biol. Chem., June 25, 2004; 279(26): 27088 - 27097.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
B. Chandrasekar, K. Vemula, R. M. Surabhi, M. Li-Weber, L. B. Owen-Schaub, L. E. Jensen, and S. Mummidi
Activation of Intrinsic and Extrinsic Proapoptotic Signaling Pathways in Interleukin-18-mediated Human Cardiac Endothelial Cell Death
J. Biol. Chem., May 7, 2004; 279(19): 20221 - 20233.
[Abstract] [Full Text] [PDF]


Home page
FASEB J.Home page
F. R. DANESH and Y. S. KANWAR
Modulatory effects of HMG-CoA reductase inhibitors in diabetic microangiopathy
FASEB J, May 1, 2004; 18(7): 805 - 815.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Renal Physiol.Home page
B. Rodriguez-Iturbe, N. D. Vaziri, J. Herrera-Acosta, and R. J. Johnson
Oxidative stress, renal infiltration of immune cells, and salt-sensitive hypertension: all for one and one for all
Am J Physiol Renal Physiol, April 1, 2004; 286(4): F606 - F616.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
C. S. Powell, M. M. Wright, and R. M. Jackson
p38mapk and MEK1/2 inhibition contribute to cellular oxidant injury after hypoxia
Am J Physiol Lung Cell Mol Physiol, April 1, 2004; 286(4): L826 - L833.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
C. Kupatt, R. Hinkel, J. Horstkotte, M. Deiss, M.-L. von Bruhl, M. Bilzer, and P. Boekstegers
Selective retroinfusion of GSH and cariporide attenuates myocardial ischemia-reperfusion injury in a preclinical pig model
Cardiovasc Res, February 15, 2004; 61(3): 530 - 537.
[Abstract] [Full Text] [PDF]


Home page
StrokeHome page
T. M. Paravicini, S. Chrissobolis, G. R. Drummond, and C. G. Sobey
Increased NADPH-Oxidase Activity and Nox4 Expression During Chronic Hypertension Is Associated With Enhanced Cerebral Vasodilatation to NADPH In Vivo
Stroke, February 1, 2004; 35(2): 584 - 589.
[Abstract] [Full Text] [PDF]


Home page
Circ. Res.Home page
J. Hwang, M. H. Ing, A. Salazar, B. Lassegue, K. Griendling, M. Navab, A. Sevanian, and T. K. Hsiai
Pulsatile Versus Oscillatory Shear Stress Regulates NADPH Oxidase Subunit Expression: Implication for Native LDL Oxidation
Circ. Res., December 12, 2003; 93(12): 1225 - 1232.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
S. S. Barbieri, S. Eligini, M. Brambilla, E. Tremoli, and S. Colli
Reactive oxygen species mediate cyclooxygenase-2 induction during monocyte to macrophage differentiation: critical role of NADPH oxidase
Cardiovasc Res, October 15, 2003; 60(1): 187 - 197.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Cell Physiol.Home page
D. Gregg, F. M. Rauscher, and P. J. Goldschmidt-Clermont
Rac regulates cardiovascular superoxide through diverse molecular interactions: more than a binary GTP switch
Am J Physiol Cell Physiol, October 1, 2003; 285(4): C723 - C734.
[Abstract] [Full Text] [PDF]


Home page
Toxicol SciHome page
H.-P. Tzeng, R.-S. Yang, T.-H. Ueng, S.-Y. Lin-Shiau, and S.-H. Liu
Motorcycle Exhaust Particulates Enhance Vasoconstriction in Organ Culture of Rat Aortas and Involve Reactive Oxygen Species
Toxicol. Sci., September 1, 2003; 75(1): 66 - 73.
[Abstract] [Full Text] [PDF]


Home page
Nephrol Dial TransplantHome page
M. Tepel
Oxidative stress: does it play a role in the genesis of essential hypertension and hypertension of uraemia?
Nephrol. Dial. Transplant., August 1, 2003; 18(8): 1439 - 1442.
[Full Text] [PDF]


Home page
Mol. Cell. Biol.Home page
N. Lopes, D. Gregg, S. Vasudevan, H. Hassanain, P. Goldschmidt-Clermont, and H. Kovacic
Thrombospondin 2 Regulates Cell Proliferation Induced by Rac1 Redox-Dependent Signaling
Mol. Cell. Biol., August 1, 2003; 23(15): 5401 - 5408.
[Abstract] [Full Text] [PDF]


Home page
Nephrol Dial TransplantHome page
M. Tepel
Oxidative stress: does it play a role in the genesis of essential hypertension and hypertension of uraemia?
Nephrol. Dial. Transplant., August 1, 2003; 18(88): 1439 - 1442.
[Full Text]


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
B. Lassegue and R. E. Clempus
Vascular NAD(P)H oxidases: specific features, expression, and regulation
Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2003; 285(2): R277 - R297.
[Abstract] [Full Text] [PDF]


Home page
Circ. Res.Home page
K. Strehlow, S. Rotter, S. Wassmann, O. Adam, C. Grohe, K. Laufs, M. Bohm, and G. Nickenig
Modulation of Antioxidant Enzyme Expression and Function by Estrogen
Circ. Res., July 25, 2003; 93(2): 170 - 177.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
J. Minners, C. J. McLeod, and M. N. Sack
Mitochondrial plasticity in classical ischemic preconditioning--moving beyond the mitochondrial KATP channel
Cardiovasc Res, July 1, 2003; 59(1): 1 - 6.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
D. D. Bannerman and S. E. Goldblum
Mechanisms of bacterial lipopolysaccharide-induced endothelial apoptosis
Am J Physiol Lung Cell Mol Physiol, June 1, 2003; 284(6): L899 - L914.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
F. Esposito, G. Chirico, N. M. Gesualdi, I. Posadas, R. Ammendola, T. Russo, G. Cirino, and F. Cimino
Protein Kinase B Activation by Reactive Oxygen Species Is Independent of Tyrosine Kinase Receptor Phosphorylation and Requires Src Activity
J. Biol. Chem., May 30, 2003; 278(23): 20828 - 20834.
[Abstract] [Full Text] [PDF]


Home page
Postgrad. Med. J.Home page
Z S Nedeljkovic, N Gokce, and J Loscalzo
Mechanisms of oxidative stress and vascular dysfunction
Postgrad. Med. J., April 1, 2003; 79(930): 195 - 200.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
G. Basta, L. Venneri, G. Lazzerini, E. Pasanisi, M. Pianelli, N. Vesentini, S. Del Turco, C. Kusmic, and E. Picano
In vitro modulation of intracellular oxidative stress of endothelial cells by diagnostic cardiac ultrasound
Cardiovasc Res, April 1, 2003; 58(1): 156 - 161.
[Abstract] [Full Text] [PDF]


Home page
Mol. Cell. Biol.Home page
G. D. Frank, M. Mifune, T. Inagami, M. Ohba, T. Sasaki, S. Higashiyama, P. J. Dempsey, and S. Eguchi
Distinct Mechanisms of Receptor and Nonreceptor Tyrosine Kinase Activation by Reactive Oxygen Species in Vascular Smooth Muscle Cells: Role of Metalloprotease and Protein Kinase C-{delta}
Mol. Cell. Biol., March 1, 2003; 23(5): 1581 - 1589.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Cell Physiol.Home page
M. Walia, S. E. Samson, T. Schmidt, K. Best, M. Whittington, C. Y. Kwan, and A. K. Grover
Peroxynitrite and nitric oxide differ in their effects on pig coronary artery smooth muscle
Am J Physiol Cell Physiol, March 1, 2003; 284(3): C649 - C657.
[Abstract] [Full Text] [PDF]


Home page
Clin. Cancer Res.Home page
J.-H. Park, T.-Y. Kim, H.-S. Jong, T. Y. Kim, Y.-S. Chun, J.-W. Park, C.-T. Lee, H. C. Jung, N. K. Kim, and Y.-J. Bang
Gastric Epithelial Reactive Oxygen Species Prevent Normoxic Degradation of Hypoxia-inducible Factor-1{alpha} in Gastric Cancer Cells
Clin. Cancer Res., January 1, 2003; 9(1): 433 - 440.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Crit. Care Med.Home page
H. J. Forman and M. Torres
Reactive Oxygen Species and Cell Signaling: Respiratory Burst in Macrophage Signaling
Am. J. Respir. Crit. Care Med., December 15, 2002; 166(12): S4 - 8.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
S. Saito, G. D. Frank, M. Mifune, M. Ohba, H. Utsunomiya, E. D. Motley, T. Inagami, and S. Eguchi
Ligand-independent trans-Activation of the Platelet-derived Growth Factor Receptor by Reactive Oxygen Species Requires Protein Kinase C-delta and c-Src
J. Biol. Chem., November 15, 2002; 277(47): 44695 - 44700.
[Abstract] [Full Text] [PDF]


Home page
Mol. Pharmacol.Home page
U. G. B. Haider, D. Sorescu, K. K. Griendling, A. M. Vollmar, and V. M. Dirsch
Resveratrol Suppresses Angiotensin II-Induced Akt/Protein Kinase B and p70 S6 Kinase Phosphorylation and Subsequent Hypertrophy in Rat Aortic Smooth Muscle Cells
Mol. Pharmacol., October 1, 2002; 62(4): 772 - 777.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
Q. Hu, Z.-X. Yu, V. J. Ferrans, K. Takeda, K. Irani, and R. C. Ziegelstein
Critical Role of NADPH Oxidase-derived Reactive Oxygen Species in Generating Ca2+ Oscillations in Human Aortic Endothelial Cells Stimulated by Histamine
J. Biol. Chem., August 30, 2002; 277(36): 32546 - 32551.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
W. Martinet, M. W.M. Knaapen, G. R.Y. De Meyer, A. G. Herman, and M. M. Kockx
Elevated Levels of Oxidative DNA Damage and DNA Repair Enzymes in Human Atherosclerotic Plaques
Circulation, August 20, 2002; 106(8): 927 - 932.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
Y. Shizukuda and P. M. Buttrick
Oxygen free radicals and heart failure: new insight into an old question
Am J Physiol Lung Cell Mol Physiol, August 1, 2002; 283(2): L237 - L238.
[Full Text] [PDF]


Home page
FASEB J.Home page
G. NICKENIG, S. BAUDLER, C. MULLER, C. WERNER, N. WERNER, H. WELZEL, K. STREHLOW, and M. BOHM
Redox-sensitive vascular smooth muscle cell proliferation is mediated by GKLF and Id3 in vitro and in vivo
FASEB J, July 1, 2002; 16(9): 1077 - 1086.
[Abstract] [Full Text] [PDF]


Home page
NEJMHome page
J. R. Sowers
Hypertension, Angiotensin II, and Oxidative Stress
N. Engl. J. Med., June 20, 2002; 346(25): 1999 - 2001.
[Full Text] [PDF]


Home page
CirculationHome page
C. Mueller, S. Baudler, H. Welzel, M. Bohm, and G. Nickenig
Identification of a Novel Redox-Sensitive Gene, Id3, Which Mediates Angiotensin II-Induced Cell Growth
Circulation, May 21, 2002; 105(20): 2423 - 2428.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
M. Potente, U. R. Michaelis, B. Fisslthaler, R. Busse, and I. Fleming
Cytochrome P450 2C9-induced Endothelial Cell Proliferation Involves Induction of Mitogen-activated Protein (MAP) Kinase Phosphatase-1, Inhibition of the c-Jun N-terminal Kinase, and Up-regulation of Cyclin D1
J. Biol. Chem., May 3, 2002; 277(18): 15671 - 15676.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
C. Kumaran and K. Shivakumar
Calcium- and superoxide anion-mediated mitogenic action of substance P on cardiac fibroblasts
Am J Physiol Heart Circ Physiol, May 1, 2002; 282(5): H1855 - H1862.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
M. Katsuyama, C. Fan, and C. Yabe-Nishimura
NADPH Oxidase Is Involved in Prostaglandin F2alpha -induced Hypertrophy of Vascular Smooth Muscle Cells. INDUCTION OF NOX1 BY PGF2alpha
J. Biol. Chem., April 12, 2002; 277(16): 13438 - 13442.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Cell Physiol.Home page
C. Li and R. M. Jackson
Reactive species mechanisms of cellular hypoxia-reoxygenation injury
Am J Physiol Cell Physiol, February 1, 2002; 282(2): C227 - C241.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
H. P. Souza, X. Liu, A. Samouilov, P. Kuppusamy, F. R. M. Laurindo, and J. L. Zweier
Quantitation of superoxide generation and substrate utilization by vascular NAD(P)H oxidase
Am J Physiol Heart Circ Physiol, February 1, 2002; 282(2): H466 - H474.
[Abstract] [Full Text] [PDF]


Home page
FASEB J.Home page
F. TOSETTI, N. FERRARI, S. DE FLORA, and A. ALBINI
Angioprevention': angiogenesis is a common and key target for cancer chemopreventive agents
FASEB J, January 1, 2002; 16(1): 2 - 14.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
X.-m. Liu, G. B. Chapman, H. Wang, and W. Durante
Adenovirus-Mediated Heme Oxygenase-1 Gene Expression Stimulates Apoptosis in Vascular Smooth Muscle Cells
Circulation, January 1, 2002; 105(1): 79 - 84.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
C. Berry, R. Touyz, A. F. Dominiczak, R. C. Webb, and D. G. Johns
Angiotensin receptors: signaling, vascular pathophysiology, and interactions with ceramide
Am J Physiol Heart Circ Physiol, December 1, 2001; 281(6): H2337 - H2365.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
G. Zalba, G. S. Jose, M. U. Moreno, M. A. Fortuno, A. Fortuno, F. J. Beaumont, and J. Diez
Oxidative Stress in Arterial Hypertension: Role of NAD(P)H Oxidase
Hypertension, December 1, 2001; 38(6): 1395 - 1399.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
L. Rossig, J. Hoffmann, B. Hugel, Z. Mallat, A. Haase, J.-M. Freyssinet, A. Tedgui, A. Aicher, A. M. Zeiher, and S. Dimmeler
Vitamin C Inhibits Endothelial Cell Apoptosis in Congestive Heart Failure
Circulation, October 30, 2001; 104(18): 2182 - 2187.
[Abstract] [Full Text] [PDF]


Home page
J. Appl. Physiol.Home page
D. R. S. Steiner, N. C. Gonzalez, and J. G. Wood
Leukotriene B4 promotes reactive oxidant generation and leukocyte adherence during acute hypoxia
J Appl Physiol, September 1, 2001; 91(3): 1160 - 1167.
[Abstract] [Full Text] [PDF]


Home page
J. Appl. Physiol.Home page
M. V. Gurjar, J. DeLeon, R. V. Sharma, and R. C. Bhalla
Mechanism of inhibition of matrix metalloproteinase-9 induction by NO in vascular smooth muscle cells
J Appl Physiol, September 1, 2001; 91(3): 1380 - 1386.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
S. L. Lee, A. R. Simon, W. W. Wang, and B. L. Fanburg
H2O2 signals 5-HT-induced ERK MAP kinase activation and mitogenesis of smooth muscle cells
Am J Physiol Lung Cell Mol Physiol, September 1, 2001; 281(3): L646 - L652.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Pathol.Home page
T.-H. Hung, J. N. Skepper, and G. J. Burton
In Vitro Ischemia-Reperfusion Injury in Term Human Placenta as a Model for Oxidative Stress in Pathological Pregnancies
Am. J. Pathol., September 1, 2001; 159(3): 1031 - 1043.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
H. D. Intengan and E. L. Schiffrin
Vascular Remodeling in Hypertension: Roles of Apoptosis, Inflammation, and Fibrosis
Hypertension, September 1, 2001; 38(3): 581 - 587.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
A. D. Schecter, A. B. Berman, L. Yi, A. Mosoian, C. M. McManus, J. W. Berman, M. E. Klotman, and M. B. Taubman
HIV envelope gp120 activates human arterial smooth muscle cells
PNAS, August 10, 2001; (2001) 181328798.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
G. Lesage, S. Glaser, Y. Ueno, D. Alvaro, L. Baiocchi, N. Kanno, J. L. Phinizy, H. Francis, and G. Alpini
Regression of cholangiocyte proliferation after cessation of ANIT feeding is coupled with increased apoptosis
Am J Physiol Gastrointest Liver Physiol, July 1, 2001; 281(1): G182 - G190.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
W. Liu, Y. Liu, and W. L. Lowe Jr.
The Role of Phosphatidylinositol 3-Kinase and the Mitogen-Activated Protein Kinases in Insulin-Like Growth Factor-I-Mediated Effects in Vascular Endothelial Cells
Endocrinology, May 1, 2001; 142(5): 1710 - 1719.
[Abstract] [Full Text]


Home page
Arterioscler. Thromb. Vasc. Bio.Home page
Z. Chen, K. W. Woodburn, C. Shi, D. C. Adelman, C. Rogers, and D. I. Simon
Photodynamic Therapy With Motexafin Lutetium Induces Redox-Sensitive Apoptosis of Vascular Cells
Arterioscler Thromb Vasc Biol, May 1, 2001; 21(5): 759 - 764.
[Abstract] [Full Text] [PDF]


Home page
Journal of Renin-Angiotensin-Aldosterone SystemHome page
M.-S. Zhou, A. Adam, and L. Raij
Review: Interaction among angiotensin II, nitric oxide and oxidative stress
Journal of Renin-Angiotensin-Aldosterone System, March 1, 2001; 2(1_suppl): S59 - S63.
[PDF]


Home page
HypertensionHome page
F. C. Luft
Workshop: Mechanisms and Cardiovascular Damage in Hypertension
Hypertension, February 1, 2001; 37(2): 594 - 598.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
A. D. Schecter, A. B. Berman, L. Yi, A. Mosoian, C. M. McManus, J. W. Berman, M. E. Klotman, and M. B. Taubman
HIV envelope gp120 activates human arterial smooth muscle cells
PNAS, August 28, 2001; 98(18): 10142 - 10147.
[Abstract] [Full Text] [PDF]


Home page
Circ. Res.Home page
R. A. Forbes, C. Steenbergen, and E. Murphy
Diazoxide-Induced Cardioprotection Requires Signaling Through a Redox-Sensitive Mechanism
Circ. Res., April 27, 2001; 88(8): 802 - 809.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
G. Cuda, R. Paterno, R. Ceravolo, M. Candigliota, N. Perrotti, F. Perticone, M. C. Faniello, F. Schepis, A. Ruocco, E. Mele, et al.
Protection of Human Endothelial Cells From Oxidative Stress: Role of Ras-ERK1/2 Signaling
Circulation, February 26, 2002; 105(8): 968 - 974.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Irani, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Irani, K.
Related Collections
Right arrow Apoptosis
Right arrow Cell signalling/signal transduction
Right arrow Growth factors/cytokines
Right arrow Smooth muscle proliferation and differentiation
Right arrow Endothelium/vascular type/nitric oxide